By Miryam Naddaf Researchers have identified 13 proteins in the blood that predict how quickly or slowly a person’s brain ages compared with the rest of their body. Their study1, published in Nature Aging on 9 December, used a machine-learning model to estimate ‘brain ages’ from scans of more than 10,000 people. The authors then analysed thousands of scans alongside blood samples and found eight proteins that were associated with fast brain ageing, and five linked to slower brain ageing. “Previous studies mainly focused on the association between the proteins and the chronological age, that means the real age of the individual,” says study co-author Wei-Shi Liu, a neurologist at Fudan University in Shanghai, China. However, studying biomarkers linked to a person’s brain age could help scientists to identify molecules to target in future treatments for age-related brain diseases. “These proteins are all promising therapeutic targets for brain disorders, but it may take a long time to validate them,” says Liu. Using machine learning to analyse brain-imaging data from 10,949 people, Liu and his colleagues created a model to calculate a person’s brain age, on the basis of features such as the brain’s volume, surface area and distribution of white matter. They wanted to identify proteins that are associated with a large brain age gap — the difference between brain age and chronological age. To do this, the researchers analysed levels of 2,922 proteins in blood samples from 4,696 people, more than half of whom were female, and compared them with the same people’s brain ages derived from the scans. They identified 13 proteins that seemed to be connected with large brain age gaps, some of which are known to be involved in movement, cognition and mental health.

Keyword: Development of the Brain
Link ID: 29597 - Posted: 12.11.2024

By Grace Huckins Genes on the X and Y chromosomes—and especially those on the Y—appear to be associated with autism likelihood, according to a study focused on people who have missing or extra sex chromosomes. The findings add to the ongoing debate about whether autism’s sex bias reflects a male vulnerability, a female protective effect or other factors. “The Y chromosome is often left out of genetic discovery studies. We really have not interrogated it in [autism] studies very much,” says Matthew Oetjens, assistant professor of human genetics at Geisinger Medical Center’s Autism and Developmental Medicine Institute, who led the new work. There is a clear sex difference in autism prevalence: Men are about four times as likely as women to have a diagnosis. But uncovering the reasons for that discrepancy has proved challenging and contentious. Multiple biological factors may play a role, in addition to social factors—such as the difficult-to-measure gulfs between how boys and girls are taught to behave. Add on the possibility of diagnostic bias and the question starts to look less like a scientific problem and more like a politically toxic Gordian knot. But there are some threads that researchers can pull to disentangle these effects, as the new study illustrates. People with sex chromosome aneuploidies—or unusual combinations of sex chromosomes, such as XXY in those with Klinefelter syndrome or a single X in Turner syndrome—provide a unique opportunity to examine how adding or taking away chromosomes can affect biology and behavior. Previous studies noted high rates of autism in people with sex chromosome aneuploidies, but those analyses were subject to ascertainment bias; perhaps those people found out about their aneuploidies only after seeking support for their neurodevelopmental conditions. © 2024 Simons Foundation

Keyword: Autism; Sexual Behavior
Link ID: 29596 - Posted: 12.11.2024

By Steven Strogatz Death might seem like a pure loss, the disappearance of what makes a living thing distinct from everything else on our planet. But zoom in closer, to the cellular level, and it takes on a different, more nuanced meaning. There is a challenge in simply defining what makes an individual cell alive or dead. Scientists today are working to understand the various ways and reasons that cells disappear, and what these processes mean to biological systems. In this episode, cellular biologist Shai Shaham talks to Steven Strogatz about the different forms of cell death, their roles in evolution and disease, and why the right kinds and patterns of cell death are essential to our development and well-being. STEVE STROGATZ: In the second that it took you to hit play on this episode, a million cells in your body died. Some were programmed to expire in natural, regulated processes, such as apoptosis. Some terminated their own lives after infection, to stop viral invaders from spreading. Others suffered physical damage and went through necrosis, their membranes splitting open and their contents spilling out. We know there are nearly a dozen different ways for our cells to kick the bucket. And learning how to control these processes can make all the difference in the world to a sick patient. In this episode, we ask cellular biologist Shai Shaham (opens a new tab), how can the death of a cell help other cells around it? And how do these insights help us understand life itself? Shai is a professor at The Rockefeller University (opens a new tab), where he studies programmed cell death during animal development and the complex role that glial cells play in the nervous system. There was an example near and dear to my heart, since we work on C. elegans, which is a nematode worm. And there was a recent description of a nematode that was extracted from permafrost in Siberia where it froze about 40,000 years ago and was revived back in the lab. And so you ask yourself, was that whole organism alive or dead for 40,000 years? © 2024 Simons Foundation

Keyword: Apoptosis; Development of the Brain
Link ID: 29591 - Posted: 12.07.2024

Aswathy Ammothumkandy, Charles Liu, Michael A. Bonaguidi Your brain can still make new neurons when you’re an adult. But how does the rare birth of these new neurons contribute to cognitive function? Neurons are the cells that govern brain function, and you are born with most of the neurons you will ever have during your lifetime. While the brain undergoes most of its development during early life, specific regions of the brain continue to generate new neurons throughout adulthood, although at a much lower rate. Whether this process of neurogenesis actually happens in adults and what function it serves in the brain is still a subject of debate among scientists. Past research has shown that people with epilepsy or Alzheimer’s disease and other dementias develop fewer neurons as adults than people without these conditions. However, whether the absence of new neurons contributes to the cognitive challenges patients with these neurological disorders face is unknown. We are part of a team of stem cell researchers, neuroscientists, neurologists, neurosurgeons and neuropsychologists. Our newly published research reveals that the new neurons that form in adults’ brains are linked to how you learn from listening to other people. Researchers know that new neurons contribute to memory and learning in mice. But in humans, the technical challenges of identifying and analyzing new neurons in adult brains, combined with their rarity, had led scientists to doubt their significance to brain function. To uncover the relationship between neurogenesis in adults and cognitive function, we studied patients with drug-resistant epilepsy. These patients underwent cognitive assessments prior to and donated brain tissue during surgical procedures to treat their seizures. To see whether how many new neurons a patient had was associated with specific cognitive functions, we looked under the microscope for markers of neurogenesis. © 2010–2024, The Conversation US, Inc.

Keyword: Neurogenesis; Learning & Memory
Link ID: 29590 - Posted: 12.07.2024

Amy Fleming Nine years ago, Nikki Schultek, an active and healthy woman in her early 30s, experienced a sudden cascade of debilitating and agonising symptoms – including cognitive and breathing problems and heart arrhythmia – and was investigated for multiple sclerosis. But three brain scans and numerous X-rays later, there was still no diagnosis or treatment plan. “It was like living in a nightmare, imagining not watching my children – three and five years old – grow up,” says Schultek. Now, speaking on a video call from North Carolina, she is as bright as a button and shows no signs of degenerative brain disease. It turned out she had multiple chronic infections, including Borrelia burgdorferi bacteria, which causes Lyme disease and which had stealthily reached her brain. Antibiotics restored her health, but B burgdorferi is hard to eradicate once in the brain. She may need maintenance treatment to keep the disease at bay. Schultek is not the only person whose neurological disorder turned out to be caused by microbes in the brain. A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible. A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener. Richard Lathe, a professor of infectious medicine at the University of Edinburgh and another lead author of the paper, says these patients “were by accident found to be suffering from various fungal, bacterial or viral infections, and when they treated the patient with antifungals, antivirals or antibiotics, the dementia went away”. He, among others, has been investigating the possibility that, like the gut, the brain hosts a community of microbes – an area of largely scientifically uncharted waters, but with huge life-saving potential. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Obesity
Link ID: 29587 - Posted: 12.04.2024

By Teddy Rosenbluth Cassava Sciences, a small biotechnology company based in Austin, Texas, announced it would stop the advanced clinical trial for an experimental Alzheimer’s drug, ending a long-contested bid for regulatory approval. The company announced on Monday that the drug, simufilam, did not significantly reduce cognitive decline in people with mild to moderate Alzheimer’s disease in the trial, which enrolled more than 1,900 patients. “The results are disappointing for patients and their families who are living with this disease and physicians who have been looking for novel treatment options,” the company’s chief executive, Richard J. Barry, said in a statement. These results were unsurprising to many dementia researchers, who had questioned why the trial had been allowed to proceed in the first place, since much of the drug’s underlying science had been called into question. Studies that once seemed to support the drug have been retracted from scientific journals. A consultant researcher who helped conduct some of the drug’s foundational studies was charged with fraud by a federal grand jury for allegedly falsifying data to obtain research grants. In September, the company settled with the Securities and Exchange Commission over allegations that Cassava had made misleading statements about the results of earlier clinical trial data. However, the company neither admitted nor denied wrongdoing. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29577 - Posted: 11.27.2024

By Andrea Tamayo Kidney cells can make memories too. At least, in a metaphorical sense. Neurons have historically been the cell most associated with memory. But far outside the brain, kidney cells can also store information and recognize patterns in a similar way to neurons, researchers report November 7 in Nature Communications. “We’re not saying that this kind of memory helps you learn trigonometry or remember how to ride a bike or stores your childhood memories,” says Nikolay Kukushkin, a neuroscientist at New York University. “This research adds to the idea of memory; it doesn’t challenge the existing conceptions of memory in the brain.” In experiments, the kidney cells showed signs of what’s called a “massed-space effect.” This well-known feature of how memory works in the brain facilitates storing information in small chunks over time, rather than a big chunk at once. Outside the brain, cells of all types need to keep track of stuff. One way they do that is through a protein central to memory processing, called CREB. It, and other molecular components of memory, are found in neurons and nonneuronal cells. While the cells have similar parts, the researchers weren’t sure if the parts worked the same way. In neurons, when a chemical signal passes through, the cell starts producing CREB. The protein then turns on more genes that further change the cell, kick-starting the molecular memory machine (SN: 2/3/04). Kukushkin and colleagues set out to determine whether CREB in nonneuronal cells responds to incoming signals the same way. © Society for Science & the Public 2000–2024.

Keyword: Learning & Memory
Link ID: 29576 - Posted: 11.27.2024

By Sofia Quaglia It’s amazing what chimpanzees will do for a snack. In Congolese rainforests, the apes have been known to poke a hole into the ground with a stout stick, then grab a long stem and strip it through their teeth, making a brush-like end. Into the hole that lure goes, helping the chimps fish out a meal of termites. How did the chimps figure out this sophisticated foraging technique and others? “It’s difficult to imagine that it can just have appeared out of the blue,” said Andrew Whiten, a cultural evolution expert from the University of St. Andrews in Scotland who has studied tool use and foraging in chimpanzees. Now Dr. Whiten’s team has set out to demonstrate that advanced uses of tools are an example of humanlike cultural transmission that has accumulated over time. Where bands of apes in Central and East Africa exhibit such complex behaviors, they say, there are also signs of genes flowing between groups. They describe this as evidence that such foraging techniques have been passed from generation to generation, and innovated over time across different interconnected communities. In a study published on Thursday in the journal Science, Dr. Whiten and colleagues go as far as arguing that chimpanzees have a “tiny degree of cumulative culture,” a capability long thought unique to humans. From mammals to birds to reptiles and even insects, many animals exhibit some evidence of culture, when individuals can socially learn something from a nearby individual and then start doing it. But culture becomes cumulative over time when individuals learn from others, each building on the technique so much that a single animal wouldn’t have been able to learn all of it on its own. For instance, some researchers interpret using rocks as a hammer and anvil to open a nut as something chimpanzees would not do spontaneously without learning it socially. Humans excel at this, with individual doctors practicing medicine each day, but medicine is no one single person’s endeavor. Instead, it is an accumulation of knowledge over time. Most chimpanzee populations do not use a complex set of tools, in a specific sequence, to extract food. © 2024 The New York Times Company

Keyword: Evolution; Learning & Memory
Link ID: 29573 - Posted: 11.23.2024

By Miryam Naddaf Humans have evolved disproportionately large brains compared with our primate relatives — but this neurological upgrade came at a cost. Scientists exploring the trade-off have discovered unique genetic features that show how human brain cells handle the stress of keeping a big brain working. The work could inspire new lines of research to understand conditions such as Parkinson’s disease and schizophrenia. The study, which was posted to the bioRxiv preprint server on 15 November1, focuses on neurons that produce the neurotransmitter dopamine, which is crucial for movement, learning and emotional processing. By comparing thousands of laboratory-grown dopamine neurons from humans, chimpanzees, macaques and orangutans, researchers found that human dopamine neurons express more genes that boost the activity of damage-reducing antioxidants than do those of the other primates. The findings, which are yet to be peer-reviewed, are a step towards “understanding human brain evolution and all the potentially negative and positive things that come with it”, says Andre Sousa, a neuroscientist at the University of Wisconsin–Madison. “It's interesting and important to really try to understand what's specific about the human brain, with the potential of developing new therapies or even avoiding disease altogether in the future.” Just as walking upright has led to knee and back problems, and changes in jaw structure and diet resulted in dental issues, the rapid expansion of the human brain over evolutionary time has created challenges for its cells, says study co-author Alex Pollen, a neuroscientist at the University of California, San Francisco. “We hypothesized that the same process may be occurring, and these dopamine neurons may represent vulnerable joints.” © 2024 Springer Nature Limited

Keyword: Development of the Brain; Stress
Link ID: 29565 - Posted: 11.20.2024

By Claudia López Lloreda Fear memories serve a purpose: A mouse in the wild learns to fear the sound of footsteps, which helps it avoid predators. But in certain situations, those fear memories can also tinge neutral memories with fear, resulting in maladaptive behavior. A mouse or person, for instance, may learn to fear stimuli that should presumably be safe. This shift can occur when an existing fear memory broadens—either by recruiting inappropriate neurons into the cell ensemble that contains it or by linking up to a previously neutral memory, according to two new studies in mice, one published today and another last week. Memories are embodied in the brain through sparse ensembles of neurons, called engrams, that activate when an animal forms a new memory or recalls it later. These ensembles were thought to be “stable and permanent,” says Denise Cai, associate professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who led one of the studies. But the new findings reveal how, during times of fear and stress, memories can become malleable, either as they are brought back online or as the neurons that encode them expand. There is “this really powerful ability of stress to look back and change memories for neutral experiences that have come before by pulling them into the same neural representation or by exciting them more during offline periods,” says Elizabeth Goldfarb, assistant professor of psychiatry at the Yale School of Medicine, who was not involved in the studies. That challenges the previous dogma, Cai says. “We’ve learned that these memory ensembles are actually quite dynamic.” © 2024 Simons Foundation

Keyword: Learning & Memory; Stress
Link ID: 29563 - Posted: 11.16.2024

Ari Daniel The birds of today descended from the dinosaurs of yore. Researchers have known relatively little, however, about how the bird's brain took shape over tens of millions of years. "Birds are one of the most intelligent groups of living vertebrate animals," says Daniel Field, a vertebrate biologist at the University of Cambridge. "They really rival mammals in terms of their relative brain size and the complexity of their behaviors, social interactions, breeding displays." Now, a newly discovered fossil provides the most complete glimpse to date of the brains of the ancestral birds that once flew above the dinosaurs. The species was named Navaornis hestiae, and it's described in the journal Nature. Piecing together how bird brains evolved has been a challenge. First, most of the fossil evidence dates back to tens of millions of years before the end of the Cretaceous period when dinosaurs went extinct and birds diversified. In addition, the fossils of feathered dinosaurs that have turned up often have a key problem. "They're beautiful, but they're all like roadkill," says Luis Chiappe, a paleontologist and curator at the Natural History Museum of Los Angeles County. "They're all flattened and there are aspects that you're never going to be able to recover from those fossils." The shape and three-dimensional structure of the brain are among those missing aspects. But in 2016, Brazilian paleontologist William Nava discovered a remarkably well-preserved fossil in São Paulo state. It came from a prehistoric bird that fills in a crucial gap in understanding of how modern bird brains evolved. © 2024 npr

Keyword: Evolution; Development of the Brain
Link ID: 29561 - Posted: 11.16.2024

By Elena Renken Small may be mightier than we think when it comes to brains. This is what neuroscientist Marcella Noorman is learning from her neuroscientific research into tiny animals like fruit flies, whose brains hold around 140,000 neurons each, compared to the roughly 86 billion in the human brain. Nautilus Members enjoy an ad-free experience. Log in or Join now . In work published earlier this month in Nature Neuroscience, Noorman and colleagues showed that a small network of cells in the fruit fly brain was capable of completing a highly complex task with impressive accuracy: maintaining a consistent sense of direction. Smaller networks were thought to be capable of only discrete internal mental representations, not continuous ones. These networks can “perform more complex computations than we previously thought,” says Noorman, an associate at the Howard Hughes Medical Institute. The scientists monitored the brains of fruit flies as they walked on tiny rotating foam balls in the dark, and recorded the activity of a network of cells responsible for keeping track of head direction. This kind of brain network is called a ring attractor network, and it is present in both insects and in humans. Ring attractor networks maintain variables like orientation or angular velocity—the rate at which an object rotates—over time as we navigate, integrating new information from the senses and making sure we don’t lose track of the original signal, even when there are no updates. You know which way you’re facing even if you close your eyes and stand still, for example. After finding that this small circuit in fruit fly brains—which contains only about 50 neurons in the core of the network—could accurately represent head direction, Noorman and her colleagues built models to identify the minimum size of a network that could still theoretically perform this task. Smaller networks, they found, required more precise signaling between neurons. But hundreds or thousands of cells weren’t necessary for this basic task. As few as four cells could form a ring attractor, they found. © 2024 NautilusNext Inc.,

Keyword: Development of the Brain; Vision
Link ID: 29560 - Posted: 11.16.2024

By Angie Voyles Askham Engrams, the physical circuits of individual memories, consist of more than just neurons, according to a new study published today in Nature. Astrocytes, too, shape how some memories are stored and retrieved, the work shows. The results represent “a fundamental change” in how the neuroscience field should think about indexing memories, says lead researcher Benjamin Deneen, professor of neurosurgery at Baylor College of Medicine. “We need to reconsider the cellular, physical basis of how we store memories.” When mice form a new memory, a specific set of neurons becomes active and expresses the immediate early gene c-FOS, past work has found. Reactivating that ensemble of neurons, the engram, causes the mice to recall that memory. Interactions between neurons and astrocytes are critical for the formation of long-term memory, according to a spatial transcriptomics study from February, and both astrocytes and oligodendrocytes are involved in memory formation, other work has shown. Yet engram studies have largely ignored the activity of non-neuronal cells, says Sheena Josselyn, senior scientist at the Hospital for Sick Children, who was not involved in the new study. But astrocytes are also active alongside neurons as memories are formed and recalled, and disrupting the star-shaped cells’ function interferes with these processes, the new work reveals. The study does not dethrone neurons as the lead engram stars, according to Josselyn. “It really shows that, yes, neurons are important. But there are also other players that we’re just beginning to understand the importance of,” she says. “It’ll help broaden our focus.” © 2024 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29558 - Posted: 11.13.2024

By Sara Reardon Elephants love showering to cool off, and most do so by sucking water into their trunks and spitting it over their bodies. But an elderly pachyderm named Mary has perfected the technique by using a hose as a showerhead, much in the way humans do. The behavior is a remarkable example of sophisticated tool use in the animal kingdom. But the story doesn’t end there. Mary’s long, luxurious baths have drawn so much attention that an envious elephant at the Berlin Zoo has figured out how to shut the water off on her supersoaking rival—a type of sabotage rarely seen among animals. Both behaviors, reported today in Current Biology, further cement elephants as complex thinkers, says Lucy Bates, a behavioral ecologist at the University of Portsmouth not involved in the study. The work, she says, “suggests problem solving or even ‘insight.’” Many elephants enjoy playing with hoses, probably because they remind them of trunks, says Michael Brecht, a computational neuroscientist at Humboldt University of Berlin. But Mary takes the activity to another level. Using her trunk, the 54-year-old Asian elephant (Elephas maximus)—a senior citizen, given the average captive life span of her species of 48 years—holds a hose over her head and waves it back and forth. She also changes her grip on the hose to spray different parts of her body and swings it like a lasso to throw water over her back. Brecht’s graduate student, Lena Kaufmann, noticed Mary’s hose use while studying other types of behavior in the zoo’s elephants; the zookeepers told her Mary did this frequently. So Kaufman and her colleagues started to record the showering on video over the course of a year, testing how Mary reacted to changes in the setup.

Keyword: Learning & Memory; Evolution
Link ID: 29547 - Posted: 11.09.2024

By Heidi Ledford To unlock the secrets of human ageing, researchers might do better to look to the pet napping on their couch than to a laboratory mouse. As cats age, their brains show signs of atrophy and cognitive decline that more closely resemble the deterioration seen in ageing humans than do the changes in the brains of ageing mice, according to findings presented last month at the Lake Conference on Comparative and Evolutionary Neurobiology near Seattle, Washington. The results are part of a large project, called Translating Time, that compares brain development across more than 150 mammal species, and is now expanding to include data on aging. The hope is that the data will aid researchers trying to crack the causes of age-related diseases, particularly conditions that affect the brain, such as Alzheimer’s disease. “To address challenges in human medicine, we need to draw from a wide range of model systems,” says Christine Charvet, a comparative neuroscientist at Auburn University College of Veterinary Medicine in Alabama, who presented the work. “Cats, lemurs, mice are all useful. We shouldn’t focus all our efforts on one.” The Translating Time project started in the 1990s as a tool for developmental biologists1. Project scientists compiled data on how long it takes for the brain to reach a range of developmental milestones in a variety of mammals and used these data to graph the relative development of two species over time. This can help researchers to link observations of animal development to the corresponding human age. Over the years, however, as Charvet presented these data at conferences, researchers kept asking her to extend the database to include not only early development, but also how the brain changes as animals age. © 2024 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 29545 - Posted: 11.06.2024

By Thomas Fuller Over and over, the crows attacked Lisa Joyce as she ran screaming down a Vancouver street. They dive bombed, landing on her head and taking off again eight times by Ms. Joyce’s count. With hundreds of people gathered outdoors to watch fireworks that July evening, Ms. Joyce wondered why she had been singled out. “I’m not a fraidy-cat, I’m not generally nervous of wildlife,” said Ms. Joyce, whose crow encounters grew so frequent this past summer that she changed her commute to work to avoid the birds. “But it was so relentless,” she said, “and quite terrifying.” Ms. Joyce is far from alone in fearing the wrath of the crow. CrowTrax, a website started eight years ago by Jim O’Leary, a Vancouver resident, has since received more than 8,000 reports of crow attacks in the leafy city, where crows are relatively abundant. And such encounters stretch well beyond the Pacific Northwest. A Los Angeles resident, Neil Dave, described crows attacking his house, slamming their beaks against his glass door to the point where he was afraid it would shatter. Jim Ru, an artist in Brunswick, Maine, said crows destroyed the wiper blades of dozens of cars in the parking lot of his senior living apartment complex. Nothing seemed to dissuade them. Renowned for their intelligence, crows can mimic human speech, use tools and gather for what seem to be funeral rites when a member of their murder, as groups of crows are known, dies or is killed. They can identify and remember faces, even among large crowds. They also tenaciously hold grudges. When a murder of crows singles out a person as dangerous, its wrath can be alarming, and can be passed along beyond an individual crow’s life span of up to a dozen or so years, creating multigenerational grudges. © 2024 The New York Times Company

Keyword: Intelligence; Learning & Memory
Link ID: 29534 - Posted: 10.30.2024

By RJ Mackenzie Microglia were once thought to have one job—as the brain’s resident garbage collectors. If neurons became damaged or diseased, microglia would spring into action, engulfing dead or infected cells and pumping up the local immune response. Between clean-up operations, scientists believed, they rested in a deep sleep. In 2005, though, researchers got their first direct look at what microglia were doing in the brain, and they promptly tore up this cellular CV. The grainy live-cell imaging footage, published in Science, showed that the supposedly “resting” microglia were actually marauding around in the neocortex of adult mice, firing out processes and furtively feeling out the surrounding parenchyma. “This, for me, was a game changer,” says Rosa Paolicelli, associate professor of biomedical sciences at the University of Lausanne, who was about to embark on a Ph.D. at the time. “People started to think about the physiological role of microglia. What do they do in the intact, healthy brain?” The work kick-started two decades of research that has changed how the field classifies microglia, and led to new tools to help scientists define and scrutinize the cells’ functions in detail. Many studies have focused on “critical windows”—at the beginning and end of an animal’s life, Paolicelli says. During these time frames, microglia take on many side jobs: as sculptors of the developing brain, cultivators of new neural connections and fighters of neurodegeneration, for example. Along with this rise in profile from garbage collector to cellular polymath has come controversy. “There are some players that are trying to bring forward some ideas that are a bit too simplistic or restrictive. And I feel it’s very dangerous not to stay open-minded regarding the implications of the findings, not to stay open-minded regarding the limitations of all these models,” says Marie-Ève Tremblay, professor of medical sciences at the University of Victoria, who studies microglial function in health and disease. © 2024 Simons Foundation

Keyword: Glia; Learning & Memory
Link ID: 29533 - Posted: 10.30.2024

Emily Anthes In the summer of 2018, off the coast of British Columbia, an orca named Tahlequah gave birth. When the calf died after just half an hour, Tahlequah refused to let go. For more than two weeks, she carried her calf’s body around, often balancing it on her nose as she swam. The story went viral, which came as no surprise to Susana Monsó, a philosopher of animal minds at the National Distance Education University in Madrid. Despite the vast chasm that seems to separate humans and killer whales, this orca mother was behaving in a way that was profoundly relatable. “This idea of a mother clinging on to the corpse of her baby for 17 days seems like something we can understand, something we can relate to, for those of us who have experienced loss,” Dr. Monsó said. Of course, projecting our own human experiences onto other species can be a tricky business, and scientists often warn about the mistakes we can make when we engage in this sort of anthropomorphism. But we can also be misled by our tendency to assume that many cognitive and emotional traits are unique to humans, Dr. Monsó said. And in her new book, “Playing Possum,” she argues that a variety of animal species have at least a rudimentary concept of death. Dr. Monsó spoke with The New York Times about her work. This conversation has been condensed and edited for clarity. How did you get interested in this aspect of animal minds? I’ve always been interested in those capacities that are understood to be uniquely human, such as morality or rationality. Death was a natural topic to pick up. There had been a growing number of reports of animals reacting in different ways to corpses. This seemed to be the birth of a new discipline, which is called comparative thanatology: the study of animals’ relationship with death. © 2024 The New York Times Company

Keyword: Intelligence; Animal Communication
Link ID: 29530 - Posted: 10.30.2024

By Jennifer Couzin-Frankel Two esteemed hospitals in the midwestern United States are a 5-hour drive apart, but when it comes to how they’re prescribing new drugs for Alzheimer’s disease, they might as well be on different planets. “I’ve been worrying about these therapies for a long time,” says Alberto Espay, a neurologist at the University of Cincinnati Medical Center, where, to his knowledge, not a single patient has gotten the monoclonal antibody lecanemab or its more recently approved cousin donanemab. Both therapies clear the brain of the protein beta amyloid, which is widely thought to fuel the disease’s symptoms. In June, Espay wrote to his Alzheimer’s patients urging them to steer clear. “The risks are high,” his letter said, citing brain swelling and bleeding. “True benefits are minuscule.” But travel a few states west, to Washington University in St. Louis (WUSTL), and the vibe is completely different. “Any patient I see with mild Alzheimer’s disease, I’m at least asking myself, ‘Should we recommend this?’” says Joy Snider, a neurologist at the university, where 230 people have received lecanemab. (Donanemab isn’t widely available yet.) “We don’t want to overplay these drugs,” Snider says. “It’s a small effect, but it’s compelling.” The contrasting views underscore deep divisions and uncertainty. The treatments are the first that have been shown to change the course of a shattering and ultimately deadly disease. But their effectiveness is under debate and they can cause sometimes severe brain swelling and bleeding. Clinicians at centers offering the drugs meet regularly to discuss patient side effects, consider whether people with other health conditions can safely get the treatments, and experiment with lower doses or extra monitoring for higher risk patients. As Alzheimer’s experts converge in Madrid this week for the Clinical Trials on Alzheimer’s Disease (CTAD) conference, the antibodies’ real-world rollout is causing a stir.

Keyword: Alzheimers
Link ID: 29529 - Posted: 10.30.2024

By Walt Bogdanich and Carson Kessler By 2021, nearly 2,000 volunteers had answered the call to test an experimental Alzheimer’s drug known as BAN2401. For the drugmaker Eisai, the trial was a shot at a windfall — potentially billions of dollars — for defanging a disease that had confounded researchers for more than a century. To assess the drug’s effectiveness and safety, Eisai sought to include people whose genetic profiles made them especially prone to develop Alzheimer’s. But these same people were also more vulnerable to brain bleeding or swelling if they received the drug. To identify these high-risk volunteers, Eisai told everyone that they would be given a genetic test. But the results, the company added, would remain secret. In all, 274 volunteers joined the trial without Eisai telling them they were at an especially high risk for brain injuries, documents obtained by The New York Times show. One of them was Genevieve Lane, a 79-year-old resident of the Villages in Florida who died in September 2022 after three doses of the drug, her brain riddled with 51 microhemorrhages. An autopsy determined that the drug’s side effects had contributed to her death. Her final hours were spent thrashing so violently that nurses had to tie her down. Another high-risk trial volunteer died, and more than 100 others suffered brain bleeding or swelling. While most of those injuries were mild and asymptomatic, some were serious and life-threatening. “This is a medication that has some significant side effects, and we need to be aware of them,” said Dr. Matthew Schrag, the Vanderbilt University neurologist who assisted with Ms. Lane’s autopsy. This past July, the agency approved a second, similar drug, Kisunla. In a clinical trial, its maker, Eli Lilly, also chose not to tell 289 volunteers that their genetic profiles made them vulnerable to brain injuries, The Times found. Dozens experienced what Lilly classified as “severe” brain bleeding. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29528 - Posted: 10.26.2024